The mechanisms that control the release of antidiuretic hormone (ADH) in normal individuals appear to be a complex interplay of osmoreceptor and cardiovascular volume receptor activity. Inferential evidence currently available would suggest that volume of stretch receptors play a prime role in the regulation of bloodADH levels and thus water homeostasis. Manipulations presumed to alter atrial filling, such as positional changes, have been shown to have significant effects on blood ADH levels in normal subjects. The experiments we are pursuing are designed to study the effects of a variety of diseases on the volume regulatory mechanisms for ADH. Our studies have shown that pneumonia and status asthmaticus are associated with elevated plasma ADH levels presumably because these disease entities interfere with left atrial filling. Patients with right and left cardiac failure are also being investigated. The studies suggest that plasma ADH levels is not elevated in left heart failure but probably is high in right heart failure and may, thereby, contribute to the development of hyponatremia in these patients.